Investigation of neural and biomechanical impairments leading to pathological toe and heel gaits using neuromusculoskeletal modelling

Bruel, Alice; Ghorbel, Salim Ben; Russo, Andrea Di; Stanev, Dimitar; Armand, Stéphane; Courtine, Grégoire; Ijspeert, Auke Jan

doi:10.1113/jp282609

Cited by 13 publications

(21 citation statements)

References 80 publications

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“…We found no exclusive effect of the investigated muscle weakness on pathological gait in SPG4 patients, which might be explained by the still remaining isometric force of more than 40%. Bruel et al (2022 ) showed that increased velocity- and force-related sensory-motor reflexes of GAS and SOL lead to pathological toe-walking patterns, which can be seen in later stages of manifest spastic patients. Furthermore, Jansen et al (2014 ) used hyper-excitability of muscle spindle length- and velocity reflex loops to simulate hemiparetic gait in a neuro-musculoskeletal model.…”

Section: Discussionmentioning

confidence: 99%

“…We introduced this cost function, since we were interested in the subtle gait changes of prodromal and early-to-moderate SPG4 subjects, who still perform a heel strike walking pattern. To simulate more severe stages of SPG4, a different cost function may be needed, to allow a less constrained gait pattern ( Bruel et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

“…We used a neuro-musculo-skeletal model of human gait, as it was used recently by Bruel et al (2022 ). The model is planar (sagittal plane) with seven segments (trunk-pelvis, bilateral thigh, lower-leg, and foot) and seven degrees of freedom (simplified from OpenSim gait2392 ( Delp et al, 2007 )).…”

Section: Methodsmentioning

confidence: 99%

“…Jansen et al (2014 ) showed how hyperexcitability of muscle spindle reflex loops contribute to hemiparetic gait by investigating length- and velocity feedback. Bruel et al (2022 ) combine the effects of muscle weakness and hyperreflexia to explain the sensory-motor origin of the spastic heel- and toe-walking. In their study, they added muscle spindle-, length-, and force feedback to the two plantarflexor muscles, Soleus (SOL) and Gastrocnemius medialis (GAS), and introduced muscle weakness by reducing the maximum isometric muscle forces ( Bruel et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

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Dysfunctional neuro-muscular mechanisms explain gradual gait changes in prodromal spastic paraplegia

Laßmann

Ilg

Rattay

et al. 2022

Preprint

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In Hereditary Spastic Paraplegia (HSP) type 4 (SPG4) a length-dependent axonal degeneration in the cortico-spinal tract leads to progressing symptoms of hyperreflexia, muscle weakness, and spasticity of lower extremities. Even before the manifestation of spastic gait, in the prodromal phase, axonal degeneration leads to subtle gait changes. These gait changes - depicted by digital gait recording - are related to disease severity in prodromal and early-to-moderate manifest SPG4 subjects. We hypothesize that dysfunctional neuro-muscular mechanisms such as hyperreflexia and muscle weakness explain these disease severity-related gait changes of prodromal and early-to-moderate manifest SPG4 subjects. We test our hypothesis in computer simulation with a neuro-muscular model of human walking. We introduce neuro-muscular dysfunction by gradually increasing sensory-motor reflex sensitivity based on increased velocity feedback and gradually increasing muscle weakness by reducing maximum isometric force. By increasing hyperreflexia of plantarflexor and dorsiflexor muscles, we found gradual muscular and kinematic changes in neuro-musculoskeletal simulations that are comparable to subtle gait changes found in prodromal SPG4 subjects. Predicting kinematic changes of prodromal and early-to-moderate manifest SPG4 subjects by gradual alterations of sensory-motor reflex sensitivity allows us to link gait as a directly accessible performance marker to emerging neuro-muscular changes for early therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dysfunctional neuro-muscular mechanisms explain gradual gait changes in prodromal spastic paraplegia

Laßmann

Ilg

Rattay

et al. 2022

Preprint

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“…Further suggestions could be provided in investigating pathological gaits. Past studies tried reproducing neural pathologies with neuromechanical simulation by extending previous controllers, in-cluding specific connections to model the pathology in the desired degree of freedom [6]. However, the controller proposed could be more suitable for studying neuropathologies like hyperreflexia considering the effects of both excessive inputs from Ia fibers and the lack of reciprocal inhibition.…”

Section: Speedmentioning

confidence: 99%

Investigating the roles of reflexes and central pattern generators in the control and modulation of human locomotion using a physiologically plausible neuromechanical model

Russo

Stanev

Sabnis

et al. 2023

Preprint

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Studying the neural components regulating movement in human locomotion is obstructed by the inability to perform invasive experimental recording. Neuromechanical simulations can provide insights by modeling the locomotor circuits. Past neuromechanical models proposed control of locomotion either driven by central pattern generators (CPGs) with simple sensory commands or by a purely reflex-based network regulated by state-machine mechanisms. However, the physiological interpretation of these state-machines remains unclear. Here, we present a physiologically plausible model to investigate spinal control and modulation of human locomotion. We propose a bio-inspired controller composed of two coupled central pattern generators (CPGs) that produce the rhythm and pattern and a reflex-based network simulating low-level reflex pathways and Renshaw cells. This reflex network is based on leaky-integration neurons, and the whole system does not rely on changing reflex gains according to the gait cycle state. The only component of the controller that maintains a state-machine mechanism is the balance controller of the trunk. The musculoskeletal model is composed of a skeletal structure and 9 muscles per leg generating movement in sagittal plane. After optimizing the open parameters, human locomotion replicating kinematics and muscle activation naturally emerged. Furthermore, when CPGs were not activated, no stable and physiologically plausible gaits could be achieved through optimization, suggesting the necessity of this component to generate rhythmic behavior without a state machine mechanism regulating reflex activation. The controller could reproduce a wide range of speeds from 0.3 to 1.9 m/s. The results also showed that the net influence of feedback on motoneurons during perturbed locomotion is predominantly inhibitory and that the CPG network provides the timing of motoneurons' activation by exciting or inhibiting muscles in specific gait phases. The proposed bio-inspired controller could contribute to our understanding of locomotor circuits of the intact spinal cord and could be used to study neuromotor disorders.

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A spinal cord neuroprosthesis for locomotor deficits due to Parkinson’s disease

Milekovic,

Moraud,

Macellari

et al. 2023

Nat Med

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NHPs were similar to those quantified in people with PD (Fig. 1h and Extended Data Fig. 1d).These results show that MPTP-treated NHPs displayed gait impairments and balance problems that share many features commonly observed in people with PD. We concluded that the MPTP-treated NHP is an appropriate preclinical model for the development of a neuroprosthesis to alleviate gait impairments and balance problems due to PD.

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Investigation of neural and biomechanical impairments leading to pathological toe and heel gaits using neuromusculoskeletal modelling

Abstract: support-information-section).

Cited by 13 publications

References 80 publications

Dysfunctional neuro-muscular mechanisms explain gradual gait changes in prodromal spastic paraplegia

Dysfunctional neuro-muscular mechanisms explain gradual gait changes in prodromal spastic paraplegia

Investigating the roles of reflexes and central pattern generators in the control and modulation of human locomotion using a physiologically plausible neuromechanical model

A spinal cord neuroprosthesis for locomotor deficits due to Parkinson’s disease

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